Guha Nilanjan, Desai Parima, Vancura Ales
Department of Biological Sciences, St. John's University, Queens, NY 11439, USA.
Mol Biol Cell. 2007 Jul;18(7):2419-28. doi: 10.1091/mbc.e06-10-0946. Epub 2007 Apr 11.
In Saccharomyces cerevisiae, many osmotically inducible genes are regulated by the Sko1p-Ssn6p-Tup1p complex. On osmotic shock, the MAP kinase Hog1p associates with this complex, phosphorylates Sko1p, and converts it into an activator that subsequently recruits Swi/Snf and SAGA complexes. We have found that phospholipase C (Plc1p encoded by PLC1) is required for derepression of Sko1p-Ssn6p-Tup1p-controlled osmoinducible genes upon osmotic shock. Although plc1Delta mutation affects the assembly of the preinitiation complex after osmotic shock, it does not affect the recruitment of Hog1p and Swi/Snf complex at these promoters. However, Plc1p facilitates osmotic shock-induced recruitment of the SAGA complex. Like plc1Delta cells, SAGA mutants are osmosensitive and display compromised expression of osmotically inducible genes. The reduced binding of SAGA to Sko1p-Ssn6p-Tup1p-repressed promoters in plc1Delta cells does not correlate with reduced histone acetylation. However, SAGA functions at these promoters to facilitate recruitment of the TATA-binding protein. The results thus provide evidence that Plc1p and inositol polyphosphates affect derepression of Sko1p-Ssn6p-Tup1p-controlled genes by a mechanism that involves recruitment of the SAGA complex and TATA-binding protein.
在酿酒酵母中，许多渗透诱导基因受Sko1p-Ssn6p-Tup1p复合物调控。在渗透应激时，丝裂原活化蛋白激酶Hog1p与该复合物结合，使Sko1p磷酸化，并将其转化为激活剂，随后该激活剂招募Swi/Snf和SAGA复合物。我们发现，磷脂酶C（由PLC1编码的Plc1p）是渗透应激时Sko1p-Ssn6p-Tup1p控制的渗透诱导基因去阻遏所必需的。尽管plc1Δ突变影响渗透应激后起始前复合物的组装，但它不影响Hog1p和Swi/Snf复合物在这些启动子处的招募。然而，Plc1p促进渗透应激诱导的SAGA复合物的招募。与plc1Δ细胞一样，SAGA突变体对渗透敏感，并且渗透诱导基因的表达受损。plc1Δ细胞中SAGA与Sko1p-Ssn6p-Tup1p抑制的启动子结合减少与组蛋白乙酰化减少无关。然而，SAGA在这些启动子处发挥作用以促进TATA结合蛋白的招募。因此，结果提供了证据表明Plc1p和肌醇多磷酸通过涉及招募SAGA复合物和TATA结合蛋白的机制影响Sko1p-Ssn6p-Tup1p控制基因的去阻遏。
